Broad Complex Tachycardias

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Broad Complex Tachycardias

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A tachycardia is defined as a heart rate greater than 100 beats per minute (bpm).

In broad complex tachycardias the QRS complex is longer than 120 ms (three small squares on the ECG).[1]

A broad QRS complex is either caused by the ventricular conducting system not working (bundle branch block) or the electrical circuit not involving the atrioventricular (AV) node correctly. Broad complex tachycardias may be ventricular or supraventricular in origin.

Aberrant conduction usually manifests as either left or right bundle branch block and the bundle branch block may predate the tachycardia.

It may be a rate-related functional block, occurring when atrial impulses arrive too rapidly for a bundle branch to conduct normally.

Wolff-Parkinson-White syndrome: in the Wolff-Parkinson-White syndrome the atrial impulses are conducted down the accessory pathway, which may allow rapid conduction and consequently very fast ventricular rates with broad QRS complexes. The QRS pattern is fairly constant, except for occasional normal complexes and fusion beats.

Atrial fibrillation: broad complex tachycardias may occur, either as an atrioventricular re-entrant tachycardia or in association with atrial flutter or atrial fibrillation.

Presentation

A ventricular origin for a broad complex tachycardia is suggested if the patient is aged over 35 years and has a history of ischaemic heart disease or congestive cardiac failure.

Symptoms

Depend on the haemodynamic consequences of the arrhythmia rather than the origin of the arrhythmia.

In some patients with VT, they may not be in a state of collapse, but present with dizziness, palpitations, syncope, chest pain or heart failure.

Some patients with SVT and poor ventricular function may present in a state of haemodynamic collapse.

Signs

In VT the rhythm is regular or almost regular.

An obviously irregular rhythm is most likely due to atrial fibrillation with either aberrant conduction or pre-excitation.

Clinical evidence of atrioventricular dissociation, ie cannon waves in the jugular venous pulse or variable intensity of the first heart sound, indicates a VT.

Physical signs will also vary according to the haemodynamic effects of the tachycardia.

Investigations

Usually shows monomorphic QRS complexes as seen in most common forms of sustained VT.

QRS complex shape is unusual and of prolonged duration (usually >0.12 seconds). Normally, the longer the duration of the QRS complex the more likely it is to be VT (particularly if >0.16 seconds). Changing QRS morphology during the tachycardia also indicates a ventricular origin.

Evidence of AV dissociation through presence of P waves independent of the QRS complex is common but not always present.

Rate: usually 120-300 bpm.

Rhythm: regular or approximately regular unless affected by capture or fusion beats. A clearly irregular rhythm it most likely to be due to AF.

Diagnostic features (absence of these does not exclude VT):

Capture beats: the sinoatrial node transiently ‘captures’ the ventricles during AV dissociation; the resulting QRS complex is of normal duration.

Fusion beats: QRS complexes somewhere between a standard QRS and the others present on the trace. They occur when a normal AV node beat fuses with a beat originating from the ventricles.

QRS concordance: all QRS complexes in chest leads either mainly positive or negative.

The treatment of a broad complex tachycardia depends on the origin of the tachycardia and should be treated as sustained VT until proven otherwise.

Vagal stimulation (eg, carotid sinus massage or the Valsalva manoeuvre) does not usually affect a VT but may affect arrhythmias of supraventricular origin. By transiently slowing or blocking conduction through the AV node, an atrioventricular nodal re-entrant tachycardia or atrioventricular re-entrant tachycardia may be terminated. In atrial flutter, transient block may reveal the underlying flutter waves.

Prognosis

Monomorphic VT usually occurs after myocardial infarction and is a sign of extensive myocardial damage; there is a high mortality, often resulting from impaired ventricular function.

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